Some direct primary causes of xerostomia are autoimmune diseases such as Sjogren's syndrome, medical irradiation, malnutrition, hormonal imbalance, arthritis and perhaps aging. When areas of the head or neck are medically irradiated by as little as 1000 rads per week, 85 percent of the patients suffer from xerostomia after six weeks and 95 percent after three months.
Secondarily, xerostomia is a side effect from the administration of over 400 drugs, including major antihypertensives, antidepressants, antispasmodics, diuretics, muscle relaxants, antipsychotics, appetite depressants, and therapeutics for Parkinson's disease.
Furthermore, xerostomia may be emotionally induced by apprehension and fear, but postponed by lascivious anticipation. Breathing through the mouth may also induce xerostomia.
Normally an individual produces 0.5 to 1 liter per day of saliva. Although varying greatly between individuals, on average 65 percent of saliva is submandibular, 23 percent from the parotids, 8 percent from the minor mucous, and 4 percent sublingual. Saliva from the different sources have different proportions of electrolytes such as sodium, potassium, calcium, magnesium, chloride, bicarbonate, phosphate, nonelectrolytes such as urea and proteins. Upon stimulation, parotid contribution increases and thus proportionally, if not actually, submandibular decreases.
Food, in general, increases salivary flow. It has been known that the effects of secondary xerostomia may be broadly alleviated by sweet, sour, or bitter foods such as sweet candies, lemon drops, peppermint drops, chewing gum, and the like.
Direct sialogogues include:
(a) pilocarpine compounds such as the hydrochloride, nitrate, or jaborandi leaves or their extracts; PA1 (b) neostigmine and its bromide, distigmine bromide (Ubretid), pyridostigmine bromide (Mestinon); PA1 (c) nicotinic acid, nicotinamide (Nicobion 500), and benzopyrone (Venalot); and PA1 (d) carbachol (Doryl), potassium iodide, and anetholthrithion (Sulfarlem S 25) PA1 ascorbic acid (Vitamin C), citric acid tablets, malic acid, lemon glycerine swabs, and paraffin wax. PA1 (a) from about 2 wgt percent to about 3 wgt percent of a food-grade, organic acidulent: PA1 (b) from about 0.05 to about 0.5 wgt percent of a food-grade synthetic sweetener or 0.5 to about 25 wgt percent of a food-grade natural sweetener; and PA1 (c) a saturated calcium phosphate solution,
Indirect sialogogues include:
The above information has been reviewed by Imfeld in volume 13, number 4, of Acta Parodontologics at pp. 1083/111-10996/124 (1984) and by Vissink et al. at volume 129, number 43 of Ned Tijdschrift Geneesked at pp. 2054-2057 (1985).
Schlatter in U.S. Pat. No. 3,492,131 discloses a family of aspartylphenylalanine esters as synthetic sweeteners about 150 times sweeter than sucrose.
Morris et al. in U.S. Pat. No. 3,584,112 teach the use of sodium saccharin sweetener to mask the taste of dental plaque-tracing dye solution.
Krasse in "Caries Risk" chapter 8, Quintessence Publ. Co., Chicago, (1985) disclosed an acidulated calcium phosphate-xylitol tablet containing citric and malic acids to be masticated and swallowed each half minute in order to stimulate salivation. Differences in chewing habits would target different salivary glands in different people.
Goodman et al. in European patent application 1984--No. 128,654 have disclosed a new class of aminoacid based sweeteners: N-(L-aspartyl)-1,1 diaminoalkanes. Goodman's group in Peptides, pp. 549-554 (1984) also emphasize that the bitter taste receptors and sweet taste receptors in the mouth are closely allied, as are the molecular arrangement of "sweet" and "bitter" compounds. These same workers in The Journal of Medicinal Chemistry, volume 27, pp. 1668-1672 (1984) disclose the close relationship between the molecular structure of sweet and bitter trifluoroacetylaspartylanilides.